Effective Quadriceps Training in Patellofemoral Pain: Difference between revisions

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# '''Swelling''':  Stoke and Young (1984) elegantly demonstrated that 40 mL of fluid can inhibit the vastus lateralis and only 10mL is needed to inhibit the VMO.<ref>Stokes M, Young A. Investigations of quadriceps inhibition: implications for clinical practice. Physiotherapy. 1984 Nov;70(11):425-8.</ref> This is clinically relevant for patients who have a small [[Effusion tests of the Knee|effusion]] in the knee status post minor knee surgery.  For example: a patient has undergone an arthroscopic meniscectomy then suddenly presents with post-operative patellofemoral pain. Often in those situations, an effusion has shut down the VMO which is driving some patellofemoral pain in conjunction with other risk factors.<ref name=":2" />
# '''Swelling''':  Stoke and Young (1984) elegantly demonstrated that 40 mL of fluid can inhibit the vastus lateralis and only 10mL is needed to inhibit the VMO.<ref>Stokes M, Young A. Investigations of quadriceps inhibition: implications for clinical practice. Physiotherapy. 1984 Nov;70(11):425-8.</ref> This is clinically relevant for patients who have a small [[Effusion tests of the Knee|effusion]] in the knee status post minor knee surgery.  For example: a patient has undergone an arthroscopic meniscectomy then suddenly presents with post-operative patellofemoral pain. Often in those situations, an effusion has shut down the VMO which is driving some patellofemoral pain in conjunction with other risk factors.<ref name=":2" />
# '''Post-dislocation, or a heavy fall onto the knee:'''  Approximately 50% of these patients, who do not have a patellar fracture, will have pain one year post injury, and often have an effusion as well. Situations such as surgery, dislocation, or trauma can set off an effusion which creates a dramatic change in the patient's dynamic stability.  
# '''Post-dislocation, or a heavy fall onto the knee:'''  Approximately 50% of these patients, who do not have a patellar fracture, will have pain one year post injury, and often have an effusion as well. Situations such as surgery, dislocation, or trauma can set off an effusion which creates a dramatic change in the patient's dynamic stability.  
# '''Presence of pain:''' This is a similar group of patients, those which have had surgery, dislocation, fall, or other trauma. Hodges et al 2009 demonstrated that if if you inject the fat pad, which is very pain sensitive, with saline, it will immediately slow the firing of the VMO. And the more you inject, then the more profound that is. So, I think we do need to look out for this subgroup, if you like, of patellofemoral pain patients who can identify as sudden onset of pain or swelling and that's an immediate big clue that they probably are a good candidate to be doing quads work. However, don't forget of course, if you have a painful knee, for whatever reason, for long enough that in itself will drive secondary VMO sluggishness, poor performance, and over time, the atrophy will create architecture change and we'll talk about the architecture change in a minute.
# '''Presence of pain:''' This is a similar group of patients, those which have had surgery, dislocation, fall, or other trauma. Hodges et al 2009 demonstrated that alterations in knee muscle activity can be caused by pain, even when that pain is of nonmuscle origin. The was done by injecting saline into the infrapatellar fat pad.  EMG activity of the VMO was measured and found to be immediately slowed after the saline injection.  
 
 
It is important to remember that if a patient has a painful knee of any etiology for long enough, it will drive secondary VMO sluggishness and poor performance.  In addition, the atrophy will create VMO muscle architecture change.


== Quadricep Muscle Architecture ==
== Quadricep Muscle Architecture ==

Revision as of 05:30, 14 August 2022

Original Editor - Stacy Schiurring based on the course by Claire Robertson

Top Contributors - Stacy Schiurring, Jess Bell and Kim Jackson

Introduction ADD IMAGE OF KNEE JOINT[edit | edit source]

Research into the cause of patellofemoral pain has been ongoing for decades. Looking back into the history of rehabilitation medicine, in the 1990's-2000's it was believed that deficits of the vastus medialis oblique (VMO) of the quadriceps was the culprit behind patellofemoral pain. Early research often used fixed cadavers rather than live subjects meaning the data had limited applicability and external validity with that literature. More recently, research has utilised electromyography (EMG) of the VMO in isolation. While studying the VMO in isolation is not entirely non useful, it limits the study's application to clinical practice.

In more recent years, research has expanded to looking up and down the kinetic chain for a more holistic cause of patellofemoral pain. While there is a large volume of research around the quadriceps, in particular the VMO, it does not link causality to the quadriceps as the most likely problem or cause of patellofemoral pain. However, this does point to a way of predicting which rehabilitation patient will have VMO related patellofemoral pain.[1]

Patellofemoral Joint Biomechanics[edit | edit source]

Please review this article for an overview of the patellofemoral joint.

Joint kinematics[edit | edit source]

The patella serves several mechanical functions.[2] It connects the muscles of knee extension to the tibia, and contributes to knee extension by transferring the force of the quadricep muscles to the tibia via the patellar tendon like a mechanical pulley.[3][2] The patella also alters the direction of the quadricep muscle force throughout knee range of motion (ROM).[2]

Overview of patellofemoral kinematics

  • At full knee extension, the patella is located above the trochlear groove of the femur. Some of its articular surface is in contact at the distal lateral facets. The patella provides approximately 30% of the total knee extension torque at full knee extension.[2]
  • During knee flexion, the patellar tendon pulls the patella into the trochlear groove which causes a slight medial translation.[3]
  • At around 30° of knee flexion, the medial facets engage in the trochlear groove. Patella flexion increases with knee flexion. With increasing knee flexion, there is increasing patellar lateral translation and lateral tilt after an initial movement in the medial direction.[3]
  • After 45° of knee flexion, the patella slowly moves into medial rotation.[3]
  • In knee flexion greater than 90°, contact occurs on the proximal half of the medial and lateral facets.[3] The patella provides approximately 13% of total knee extension torque between 90 and 120° knee flexion.[2]


In open kinetic chain movements, the patella follows the path of the tibia due to the patellar tendon insertion at the tibial tubercle. The patella glides inferiorly during knee flexion and superiorly during knee extension. With a quadriceps set the patella should move approximately 10 mm superiorly. With knee flexion, the overall pattern of patellar contact area increases and serves to distribute joint forces over a larger surface area decreasing the likelihood of injury from repetitive high compressive forces.[2]

The patella also tracks lateral-medial-lateral during knee flexion. The patella moves approximately 3mm in each direction during medial and lateral displacement. As the knee flexes, the patella glides medially and becomes centered within the trochlear groove. During knee extension from 45° to 0° the patella tilts medially. At around 30° of flexion the patella glides back laterally and maintains this position for the remaining knee flexion. The motion has been described as a "C-curve pattern."[2]

In closed kinetic chain movements the patella remains in relatively in one place within the quadriceps tendon, this means the femur move on the patella.

ADD VIDEOS OF KNEE BIOMECHANICS and OPEN vs CLOSED CHAIN

Effects of the quadriceps ADD IMAGE OF QUAD in situ[edit | edit source]

Please review the following articles for an overview of the quadricep muscles: (1) Rectus femoris, (2) Vastus lateralis, (3) Vastus medialis, and (4) Vastus intermedius.

The VMO has been the focus of much research in relation to patellofemoral pain. There are several scenarios where the VMO has no pull on the patella which causes joint dysfunction:

  1. Swelling: Stoke and Young (1984) elegantly demonstrated that 40 mL of fluid can inhibit the vastus lateralis and only 10mL is needed to inhibit the VMO.[4] This is clinically relevant for patients who have a small effusion in the knee status post minor knee surgery. For example: a patient has undergone an arthroscopic meniscectomy then suddenly presents with post-operative patellofemoral pain. Often in those situations, an effusion has shut down the VMO which is driving some patellofemoral pain in conjunction with other risk factors.[1]
  2. Post-dislocation, or a heavy fall onto the knee: Approximately 50% of these patients, who do not have a patellar fracture, will have pain one year post injury, and often have an effusion as well. Situations such as surgery, dislocation, or trauma can set off an effusion which creates a dramatic change in the patient's dynamic stability.
  3. Presence of pain: This is a similar group of patients, those which have had surgery, dislocation, fall, or other trauma. Hodges et al 2009 demonstrated that alterations in knee muscle activity can be caused by pain, even when that pain is of nonmuscle origin. The was done by injecting saline into the infrapatellar fat pad. EMG activity of the VMO was measured and found to be immediately slowed after the saline injection.


It is important to remember that if a patient has a painful knee of any etiology for long enough, it will drive secondary VMO sluggishness and poor performance. In addition, the atrophy will create VMO muscle architecture change.

Quadricep Muscle Architecture[edit | edit source]

So, believe it or not, even as recently as 2005, there was still debate going on: was the VMO even separate from the VML? So, in other words, is the VM split into two areas, the VMO and the VML? And there was a bit of debate with a couple of papers, one by Ono, one by Peeler coming out quickly disputing this. And so, I teamed up with an anatomist and we decided to try put this argument to bed by ultrasounding a large volume of knees. So, we ultrasounded 80 knees to see if we could describe the anatomy and what we found was very interesting. So, not only did we find the VMO was a separate entity, and we can say it's got a fascial plane between the VMO and the VML, it's got a different origin on the adductor muscles, different fibre orientation, different nerve distribution, so it's clearly a separate entity.

But not only did we find that, we also found that the anatomy varied a lot across the population. So, we found some people had a VMO that its fibre was around 40 degrees to the femoral axis - think about the femur really - and we found others, it was right around more at 70 degrees to the femur. We also looked at how much of the medial border of the patella had a VMO attachment. Some people, it was a third and some people, it was right down to 95% of their medial border. So we, didn't set out to look at that, but it was such an interesting finding, so we then decided to take this and run with it from a research perspective. So, we then said, well, I wonder whether this relates to how active people are? So, we then did another study - and all these studies had been published - where we looked at Tegner scoring. So, Tegner scoring simply makes, is a way of scoring how sedentary or active someone is, and we'd measure the architecture again with the ultrasound. And sure enough, we found that people that were sedentary had a smaller fibre angle and a smaller amount of insertion. And people that were very athletic, had a large angle and a large insertion.

So, what was the burning question that I then had to answer? Can we take those people with a small angle and a small insertion, can we change that with exercise? Because that was the suggestion, but we had no proof. And so, we did another study, so we took the sedentary end of the spectrum, we put them on a very basic programme to quads overload, and of course, if you're taking people who are sedentary and weaker, it's easier to overload the muscle to light fatigue, alternate days, for six weeks. And sure enough, their muscle architecture changed.

Now look, muscle architecture research is not a new concept. The first paper was in 1955, but no one had looked it in the VMO. And of course, the VMO becomes particularly interesting and relevant because it's attaching onto the patella, which is a floating bone that will move wherever the line of pull is. So, we were able to show then that with exercise, we have a way of changing the architecture of the muscle to make it preferentially a better medial stabiliser. This is really exciting because as physios, we've known for years and years that quads work tends to help people very often with knee pain. But here lies a description of what is happening and how it is doing it.

So, we then took it further. We then said, well, we wonder if there are different types of exercises that are better? So, we did a trial which was open chain versus closed chain, and we found the results of the two groups were the same. We then did another study where we looked at closed kinetic chain exercises versus closed kinetic chain with electrical stimulation and the group that had the electrical stimulation in addition had the better result. I then wanted to know what happened more long-term, so we then did a study where one group stopped, one group carried on till 12 weeks, and the third group did - after six weeks - did two exercises twice a week. And the results were very interesting. The group that stopped saw a slight reversal of their architecture, the group that carried on to 12 weeks had a little bit more gain but not as much, and the group - and this is perhaps the most interesting message from this study - that did two exercises twice a week managed to hold their architecture change.

So, how does this work? So, in essence, when you hypertrophy a muscle, you don't get more muscle fibres, the number of muscle fibres is set, but what happens is the diameter of the muscle fibres changes. So, they become fatter and as they become fatter, they push the neighbouring fibre around and change that fibre angle, that angle of pennation. And in fact, an interesting fact for you, osteoarchaeologists look at amount of, evidence of amounts of muscle attachment onto muscles to look at how active ancient civilisations were. So, in our case, as the muscle hypertrophied, it spread down the medial border of the patella and had a bigger origin, and this is what the osteoarchaeologists are looking at with other muscle groups to see how active these civilisations were. So really very, very interesting.

So, we can offer up a better quadriceps, a better VMO and I'm sure that those of you that are working with patients will be able to picture those patients who have had a fracture, or surgery, or trauma, and have almost like a hollow appearance distally at their distal medial quads and that's because that's where those fibres have become more vertical and left this sort of gap. But we can, of course, as I've been saying, we can reverse this.

Exercises[edit | edit source]

So, we're moving away from the concept of firing the VMO in isolation because we can't. Yes, we don't want to drive delay, so we don't want to exercise, ideally, in the presence of swelling and/or much pain. A tiny bit of discomfort I think we run with, but I say to my patients, no more than about a three out of 10. Not because I'm worried about harming them, but because I think I will be ineffectual.

So, we've got to take the muscle to fatigue alternate days, and we have to do that to create that hypertrophy, to give that architecture change. Now, many of the patients, and in fact, many clinicians say, but the problem is everything I try and do is painful. So, this is where an understanding of knee angles and exercise is very helpful.

So, this has been well evidenced by Steinkamp's work. So, if we take the concept of closed chain now - so squats, lunges, leg press - between zero degrees flexion and 50 degrees flexion, yes, the patellofemoral contact load goes up. Of course, if I stand up straight and I start squatting down, I will feel that that goes up. But what happens after 50 degrees is that accelerates, and the graph does this. So, if we feel more pressure, we'll get more and more and more and this is why the patients don't generally like deep squats and lunges. So, what I say is let's stay in, particularly in the earlier parts of rehabbing, that zero to 50, but load them up. So, take the humble squat. I might start with the double leg wall squat to 45 degrees if they're weak and sore. Then I might bring them on to majority one leg, perhaps put the other foot on a ball, and I will hold it statically. And then I might increase the length of the hold, so I might do four lots of a minute with 70% of the weight on one leg, but only at about 45 degrees.

Then we might come away from the wall and we might do a double leg squat, but with some weight on a barbell or dumbbells, but again, only to about 45 degrees. Then I might stick with that, but I might do it on a BOSU or something that's slightly unstable under foot. So, what we're doing is we're progressing, we're progressing, but I'm not progressing by going deeper, banging up and down into deep flexion, which is much more likely to cause irritation. And we can apply that to the leg press, we could do isometrics, but in our range between zero and 50, apply it to squat, we can even apply it to a lunge. We're just not going to go too deep until they're really getting quite nice and strong and then we can edge into the deeper ranges when hopefully they've got the resilience, the low tolerance, and they're not going to get as sore.

And then we need to think about open chain because the graph is different for open chain. So, open chain between 90 and 45, the load increases but slowly. So, in essence, it's the other way around. Then when we go from 45 degrees to zero, think about a leg extension machine, in that range, the load really escalates. So, guess what I'm going to suggest? Yup. I'm going to suggest if you do some open chain, whether it's without TheraBand, or just seated, or with some TheraBand, or on an open chain leg extension machine, then I'm going to suggest in those earlier stages working between 90 and 45.

And, of course, we can do closed chain between zero and 45 and open chain between 90 and 45, so we're getting it to work throughout the whole range, but in different ways that are more likely for you to be able to load it up hard enough to get that fatigue. Because if you don't get to the fatigue and you don't get the recovery, you won't get the hypertrophy. So, we're looking at something like four sets of eight reps to fatigue, alternate days. And once we've got the architecture change, then we might want to move that over to more endurance bias, so we get endurance capabilities as well and that slow oxidative function. So, we might switch then to more high reps, three or four sets of 20.

And ultimately, of course, we want to work synergistically with glutes so that we get nice limb control when it is good quality movement and then always, always keeping an eye on their long-term goal. So, if they want to go back to badminton, can we start incorporating some badminton-type movements and shadowing, or actually, is it football? What is it? And keeping an eye on working towards that goal that's specific to that patient is always so key.

Okay. So, if we think about quads, the message is look out for pain and/or swelling cause that's a big clue that probably the quads, the VMO are involved in this. Don't think about VMO exercises. Just think about quads exercises. If we're doing quads exercises, we're going to be working the VMO. Okay. Don't do painful exercises. So, with respect to that as well, I think if they're very sore, think about timing the exercises after pain relief. Maybe even icing beforehand. Loro's work showed that in post-surgical patients that ice first and then do their quads work was better in terms of their EMG firing, they got better recruitment. So, time of day, they might not be very sore in the morning. Can we do their quads work then? And if they are, really are that sore that they just cannot effectively exercise to fatigue then it absolutely is worth looking at blood flow restriction training, which is a way of fatiguing the muscle quicker so that we don't get so much load on the joint, but we still get that fatigue on the muscle.

Conclusion[edit | edit source]

So, let's aspire to get this fantastic architecture back in the muscle. It's great to see this work really giving us an evidence underpinning physiologically what we do when we do our quads work and make sure that you're bespoke to the patients so that you're not just giving out the same old quads' exercises. You're thinking about what makes this patient sore, what they can tolerate, ranges, load, dosage. So, sets, reps, speed of which they're doing them. Have they got the right amount of time and attention? Think about all these things. Have they had their adequate rest days? Are they too keen and they're actually doing their exercises every day? Factor in all these elements to your quadriceps exercise prescription and then I think you'll find that whether you're doing shallow squats, shallow lunges, or maybe you're doing a reverse step down, it's a lovely way of getting some eccentric function into the quads without too much patellar load. What is it this person needs? Make it bespoke, think it through, and then you're likely to get the patient on board, get effective strength work that gives you the architecture change that then hopefully provides that dynamic stability that we're after at the patellofemoral joint.

Resources[edit | edit source]

Optional Additional Reading:

References[edit | edit source]

  1. 1.0 1.1 Robertson, C. Patellofemoral Joint Programme. Effective Quadriceps Training in Patellofemoral Pain. Physioplus. 2022.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Loudon JK. Biomechanics and pathomechanics of the patellofemoral joint. International journal of sports physical therapy. 2016 Dec;11(6):820.
  3. 3.0 3.1 3.2 3.3 3.4 Wheatley MG, Rainbow MJ, Clouthier AL. Patellofemoral mechanics: a review of pathomechanics and research approaches. Current Reviews in Musculoskeletal Medicine. 2020 Jun;13(3):326-37.
  4. Stokes M, Young A. Investigations of quadriceps inhibition: implications for clinical practice. Physiotherapy. 1984 Nov;70(11):425-8.